scholarly journals Relationships between the response of the sweet taste receptor, salivation toward sweeteners, and sweetness intensity

2020 ◽  
Author(s):  
Yuko Kusakabe ◽  
Yumiko Shindo ◽  
Takayuki Kawai ◽  
Mari Maeda‐Yamamoto ◽  
Yuji Wada
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Sweet Taste Receptor ◽  
Sweetness Intensity

Interaction of suosan with the sweet taste receptor

1982 ◽  
Vol 175 (4) ◽  
pp. 266-268 ◽  
Author(s):  
Jean-Marie Tinti ◽  
Claude Nofre ◽  
Anne-Marie Peytavi
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Sweet Taste Receptor

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.

Taste Perception and Cerebral Activity in the Human Gustatory Cortex Induced by Glucose, Fructose, and Sucrose Solutions

2019 ◽  
Vol 44 (7) ◽  
pp. 435-447 ◽  
Author(s):  
Thomas Mouillot ◽  
Sophie Barthet ◽  
Lucie Janin ◽  
Camille Creteau ◽  
Hervé Devilliers ◽  
...  
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Molar Concentration ◽  
Cortical Activation ◽  
Taste Perception ◽  
Gustatory Cortex ◽  
Intensity Perception ◽  
Sucrose Solutions ◽  
Significant Difference ◽  
Sweetness Intensity

Abstract Glucose, fructose, and sucrose are important carbohydrates in Western diets with particular sweetness intensity and metabolisms. No study has compared their cerebral detection and their taste perception. Gustatory evoked potentials (GEPs), taste detection thresholds, intensity perception, and pleasantness were compared in response to glucose, fructose, and sucrose solutions at similar sweetness intensities and at identical molar concentrations. Twenty-three healthy subjects were randomly stimulated with 3 solutions of similar sweetness intensity (0.75 M of glucose, 0.47 M of fructose and 0.29 M of sucrose – sit. A), and with an identical molar concentration (0.29 M – sit. B). GEPs were recorded at gustatory cortex areas. Intensity perception and hedonic values of each solution were evaluated as were gustatory thresholds of the solutions. No significant difference was observed concerning the GEP characteristics of the solutions according to their sweetness intensities (sit. A) or their molar concentration (sit. B). In sit. A, the 3 solutions were perceived to have similar intensities and induced similar hedonic sensations. In sit. B, the glucose solution was perceived to be less intense and pleasant than the fructose and the sucrose solutions (P < 0.001) and the fructose solution was perceived to be less intense and pleasant than the sucrose (P < 0.001). Since GEP recordings were similar for glucose, fructose, and sucrose solutions whatever the concentrations, activation of same taste receptor induces similar cortical activation, even when the solutions were perceived differently. Sweet taste perception seems to be encoded by a complex chemical cerebral neuronal network.

scholarly journals Structure-function relationships of brazzein variants with altered interactions with the human sweet taste receptor

2016 ◽  
Vol 25 (3) ◽  
pp. 711-719 ◽  
Author(s):  
Kiran K. Singarapu ◽  
Marco Tonelli ◽  
John L. Markley ◽  
Fariba M. Assadi-Porter
Keyword(s):  
Structure Function ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Sweet Taste Receptor
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