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 Gpr17 signaling decreases GLP-1 secretion in GLUTag cells

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Katherine Stalbaum ◽  
Shijun Yan ◽  
Hongxia Ren
Keyword(s):  
Metabolic Regulation ◽  
Enteroendocrine Cells ◽  
Incretin Hormone ◽  
Obesity And Diabetes ◽  
The Media ◽  
Glucagon Like Peptide 1 ◽  
The Difference ◽  
G Protein Coupled ◽  
The Brain

Background and Hypothesis: The incidence of obesity and diabetes continues to rise in devastatingly high proportions, making the need for safe, affordable, and effective treatment increasingly apparent. We discovered that the orphan G protein-coupled receptor 17 (Gpr17) is expressed in endocrine cells in the brain and gut and may have an important role in metabolic regulation. Glucagon-like peptide 1 (GLP-1), an incretin hormone secreted from enteroendocrine cells, is a strong insulin secretagogue and suppresses appetite. We hypothesized that Gpr17 signaling decreases GLP-1 secretion in gut enteroendocrine cells. Experimental Design or Project Methods: In order to investigate the role of Gpr17 in GLP-1 secretion, we measured GLP-1 secretion in a murine enteroendocrine cell line (GLUTag cells) that expresses Gpr17 and the proglucagon gene and secretes GLP-1 in a regulated manner. GLUTag cells were stimulated with glucose or lipid, oleoyl-lysophosphatidylcholine (LPC), in the presence or absence of MDL29,951, a synthetic Gpr17 agonist. After a 2-hour incubation, we measured GLP-1 in the media and cell lysates to determine the percentage of secreted GLP-1. Results: Cells treated with glucose and MDL29,951 had decreased GLP-1 secretion compared to glucose alone, however, the difference was not significant. Cells treated with LPC and MDL29,951 had a significant decrease in GLP-1 secretion compared to LPC alone. Conclusion and Potential Impact: Gpr17 activation by MDL29,951 decreased GLP-1 secretion in GLUTag cells stimulated by both glucose and lipid, which supports our hypothesis that Gpr17 signaling regulates GLP-1 secretion. Therefore, Gpr17 may be a potential pharmacological target for combating obesity and diabetes.

scholarly journals Whole-Brain Mapping of the Expression Pattern of T1R2, a Subunit Specific to the Sweet Taste Receptor

2021 ◽  
Vol 15 ◽  
Author(s):  
Jea Hwa Jang ◽  
Ha Kyeong Kim ◽  
Dong Woo Seo ◽  
Su Young Ki ◽  
Soonhong Park ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Metabolic Regulation ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Taste Receptors ◽  
Sweet Taste Receptor ◽  
Sweet Taste Receptors ◽  
The Central Nervous System ◽  
A Subunit ◽  
The Brain

Chemosensory receptors are expressed primarily in sensory organs, but their expression elsewhere can permit ligand detection in other contexts that contribute to survival. The ability of sweet taste receptors to detect natural sugars, sugar alcohols, and artificial sweeteners suggests sweet taste receptors are involved in metabolic regulation in both peripheral organs and in the central nervous system. Our limited knowledge of sweet taste receptor expression in the brain, however, has made it difficult to assess their contribution to metabolic regulation. We, therefore, decided to profile the expression pattern of T1R2, a subunit specific to the sweet taste receptor complex, at the whole-brain level. Using T1r2-Cre knock-in mice, we visualized the overall distribution of Cre-labeled cells in the brain. T1r2-Cre is expressed not only in various populations of neurons, but also in glial populations in the circumventricular organs and in vascular structures in the cortex, thalamus, and striatum. Using immunohistochemistry, we found that T1r2 is expressed in hypothalamic neurons expressing neuropeptide Y and proopiomelanocortin in arcuate nucleus. It is also co-expressed with a canonical taste signaling molecule in perivascular cells of the median eminence. Our findings indicate that sweet taste receptors have unidentified functions in the brain and suggest that they may be a novel therapeutic target in the central nervous system.

scholarly journals Transformation of postingestive glucose responses after deletion of sweet taste receptor subunits or gastric bypass surgery

2012 ◽  
Vol 303 (4) ◽  
pp. E464-E474 ◽  
Author(s):  
Maartje C. P. Geraedts ◽  
Tatsuyuki Takahashi ◽  
Stephan Vigues ◽  
Michele L. Markwardt ◽  
Andongfac Nkobena ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Glycemic Control ◽  
Large Intestine ◽  
Molecular Mechanisms ◽  
Hormone Secretion ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Oral Glucose ◽  
Isolated Pancreatic Islets ◽  
Sweet Taste Receptor

The glucose-dependent secretion of the insulinotropic hormone glucagon-like peptide-1 (GLP-1) is a critical step in the regulation of glucose homeostasis. Two molecular mechanisms have separately been suggested as the primary mediator of intestinal glucose-stimulated GLP-1 secretion (GSGS): one is a metabotropic mechanism requiring the sweet taste receptor type 2 (T1R2) + type 3 (T1R3) while the second is a metabolic mechanism requiring ATP-sensitive K+(KATP) channels. By quantifying sugar-stimulated hormone secretion in receptor knockout mice and in rats receiving Roux-en-Y gastric bypass (RYGB), we found that both of these mechanisms contribute to GSGS; however, the mechanisms exhibit different selectivity, regulation, and localization. T1R3−/−mice showed impaired glucose and insulin homeostasis during an oral glucose challenge as well as slowed insulin granule exocytosis from isolated pancreatic islets. Glucose, fructose, and sucralose evoked GLP-1 secretion from T1R3+/+, but not T1R3−/−, ileum explants; this secretion was not mimicked by the KATPchannel blocker glibenclamide. T1R2−/−mice showed normal glycemic control and partial small intestine GSGS, suggesting that T1R3 can mediate GSGS without T1R2. Robust GSGS that was KATPchannel-dependent and glucose-specific emerged in the large intestine of T1R3−/−mice and RYGB rats in association with elevated fecal carbohydrate throughout the distal gut. Our results demonstrate that the small and large intestines utilize distinct mechanisms for GSGS and suggest novel large intestine targets that could mimic the improved glycemic control seen after RYGB.

scholarly journals The Role of Post-Ingestive Feedback in the Development of an Enhanced Appetite for the Orosensory Properties of Glucose over Fructose in Rats

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 807 ◽  
Author(s):  
Kevin P. Myers ◽  
Megan Y. Summers ◽  
Elizabeth Geyer-Roberts ◽  
Lindsey A. Schier
Keyword(s):  
Taste Receptor ◽  
Glucose Consumption ◽  
Sweet Taste ◽  
Taste Quality ◽  
Sensory Properties ◽  
Control Group ◽  
Sensory Property ◽  
Matched Group ◽  
Group A

The simple sugars glucose and fructose share a common “sweet” taste quality mediated by the T1R2+T1R3 taste receptor. However, when given the opportunity to consume each sugar, rats learn to affectively discriminate between glucose and fructose on the basis of cephalic chemosensory cues. It has been proposed that glucose has a unique sensory property that becomes more hedonically positive through learning about the relatively more rewarding post-ingestive effects that are associated with glucose as compared to fructose. We tested this theory using intragastric (IG) infusions to manipulate the post-ingestive consequences of glucose and fructose consumption. Food-deprived rats with IG catheters repeatedly consumed multiple concentrations of glucose and fructose in separate sessions. For rats in the “Matched” group, each sugar was accompanied by IG infusion of the same sugar. For the “Mismatched” group, glucose consumption was accompanied by IG fructose, and vice versa. This condition gave rats orosensory experience with each sugar but precluded the differential post-ingestive consequences. Following training, avidity for each sugar was assessed in brief access and licking microstructure tests. The Matched group displayed more positive evaluation of glucose relative to fructose than the Mismatched group. A second experiment used a different concentration range and compared responses of the Matched and Mismatched groups to a control group kept naïve to the orosensory properties of sugar. Consistent with results from the first experiment, the Matched group, but not the Mismatched or Control group, displayed elevated licking responses to glucose. These experiments yield additional evidence that glucose and fructose have discriminable sensory properties and directly demonstrate that their different post-ingestive effects are responsible for the experience-dependent changes in the motivation for glucose versus fructose.

scholarly journals Expression of Taste Receptor 2 Subtypes in Human Testis and Sperm

2020 ◽  
Vol 9 (1) ◽  
pp. 264 ◽  
Author(s):  
Laura Governini ◽  
Bianca Semplici ◽  
Valentina Pavone ◽  
Laura Crifasi ◽  
Camilla Marrocco ◽  
...  
Keyword(s):  
Taste Receptor ◽  
Receptor Activation ◽  
Taste Buds ◽  
The Body ◽  
Semen Parameters ◽  
Human Testis ◽  
Taste Receptors ◽  
Organ Systems

Taste receptors (TASRs) are expressed not only in the oral cavity but also throughout the body, thus suggesting that they may play different roles in organ systems beyond the tongue. Recent studies showed the expression of several TASRs in mammalian testis and sperm, indicating an involvement of these receptors in male gametogenesis and fertility. This notion is supported by an impaired reproductive phenotype of mouse carrying targeted deletion of taste receptor genes, as well as by a significant correlation between human semen parameters and specific polymorphisms of taste receptor genes. To better understand the biological and thus clinical significance of these receptors for human reproduction, we analyzed the expression of several members of the TAS2Rs family of bitter receptors in human testis and in ejaculated sperm before and after in vitro selection and capacitation. Our results provide evidence for the expression of TAS2R genes, with TAS2R14 being the most expressed bitter receptor subtype in both testis tissue and sperm cells, respectively. In addition, it was observed that in vitro capacitation significantly affects both the expression and the subcellular localization of these receptors in isolated spermatozoa. Interestingly, α-gustducin and α-transducin, two Gα subunits expressed in taste buds on the tongue, are also expressed in human spermatozoa; moreover, a subcellular redistribution of both G protein α-subunits to different sub-compartments of sperm was registered upon in vitro capacitation. Finally, we shed light on the possible downstream transduction pathway initiated upon taste receptor activation in the male reproductive system. Performing ultrasensitive droplets digital PCR assays to quantify RNA copy numbers of a distinct gene, we found a significant correlation between the expression of TAS2Rs and TRPM5 (r = 0.87), the cation channel involved in bitter but also sweet and umami taste transduction in taste buds on the tongue. Even if further studies are needed to clarify the precise functional role of taste receptors for successful reproduction, the presented findings significantly extend our knowledge of the biological role of TAS2Rs for human male fertility.

scholarly journals The Role of Bitter and Sweet Taste Receptors in Upper Airway Immunity

2015 ◽  
Vol 15 (12) ◽  
Author(s):  
Alan D. Workman ◽  
James N. Palmer ◽  
Nithin D. Adappa ◽  
Noam A. Cohen
Keyword(s):  
Upper Airway ◽  
Sweet Taste ◽  
Taste Receptors ◽  
Sweet Taste Receptors

scholarly journals EXTRAORAL SWEET TASTE RECEPTORS IN RESPIRATORY SYSTEM

2018 ◽  
Vol 18 (1) ◽  
pp. 27-33 ◽  
Author(s):  
V N Mineev ◽  
P V Brukhanova ◽  
D E Koksharova
Keyword(s):  
Diabetes Mellitus ◽  
Respiratory Tract ◽  
Antimicrobial Peptides ◽  
Respiratory System ◽  
Clinical Medicine ◽  
Sweet Taste ◽  
Scientific Basis ◽  
Taste Receptors ◽  
Sweet Taste Receptors

The possible pathogenetic role of extraoral sweet taste receptors Tas1R in respiratory system is considered. In many respects, the function of extraoral receptors for sweet taste still remains unclear. The mechanism of intracellular signal transduction at sweet taste reception is considered, as well as the molecular mechanism of interaction of Tas2R and Tas1R receptors, expressed on the same cell. Tas1R receptors in respiratory system can function as a “rheostat” to control the amount of secretion of antimicrobial peptides that is mediated by extraoral bitter taste receptors Tas2R, depending on the concentration of glucose on the surface of the airways. In diabetes mellitus, the liquid on the luminal surface of respiratory tract contains an increased concentration of glucose, which leads to overexpression of TAS1R2 / TAS1R3, inhibition of Tas2R signaling activity and to decrease in secretion of antimicrobial peptides. Clinically, the effect on glucose homeostasis in the lumen of the respiratory tract with comorbid respiratory pathology, including diabetes mellitus, is considered. A possible sequence of pathogenetic mechanisms in respiratory system, associated with extraoral sweet taste receptors is presented as a vicious circle. Research into the problem of role of the ectopic chemosensory network in clinical medicine will bring new knowledge on the predisposition to diseases, a deeper understanding of the mechanisms of their development, and will serve as a scientific basis for developing new medicinal approaches.

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 The role of dietary fat in obesity-induced insulin resistance

2016 ◽  
Vol 311 (6) ◽  
pp. E989-E997 ◽  
Author(s):  
Denise E. Lackey ◽  
Raul G. Lazaro ◽  
Pingping Li ◽  
Andrew Johnson ◽  
Angelina Hernandez-Carretero ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Caloric Intake ◽  
High Fat ◽  
Low Fat ◽  
Feeding Method ◽  
Low Fat Diet ◽  
Obesity And Diabetes

Consumption of excess calories results in obesity and insulin resistance and has been intensively studied in mice and humans. The objective of this study was to determine the specific contribution of dietary fat rather than total caloric intake to the development of obesity-associated insulin resistance. We used an intragastric feeding method to overfeed excess calories from a low-fat diet (and an isocalorically matched high-fat diet) through a surgically implanted gastric feeding tube to generate obesity in wild-type mice followed by hyperinsulinemic-euglycemic clamp studies to assess the development of insulin resistance. We show that overfeeding a low-fat diet results in levels of obesity similar to high-fat diet feeding in mice. However, despite a similar body weight, obese high-fat diet-fed mice are more insulin resistant than mice fed an isocaloric low-fat diet. Therefore, increased proportion of calories from dietary fat further potentiates insulin resistance in the obese state. Furthermore, crossover diet studies revealed that reduction in dietary fat composition improves glucose tolerance in obesity. In the context of the current obesity and diabetes epidemic, it is particularly important to fully understand the role of dietary macronutrients in the potentiation and amelioration of disease.

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