Isothermal Titration Calorimetry Study of the Interaction of Sweeteners with Fullerenols as an Artificial Sweet Taste Receptor Model

2009 ◽  
Vol 57 (7) ◽  
pp. 2945-2954 ◽  
Author(s):  
Zhong-Xiu Chen ◽  
Gang-Min Guo ◽  
Shao-Ping Deng
Keyword(s):  
Isothermal Titration Calorimetry ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Titration Calorimetry ◽  
Receptor Model ◽  
Sweet Taste Receptor

Thermodynamics of the interaction of sweeteners and lactisole with fullerenols as an artificial sweet taste receptor model

2011 ◽  
Vol 128 (1) ◽  
pp. 134-144 ◽  
Author(s):  
Zhong-Xiu Chen ◽  
Wen Wu ◽  
Wei-Bin Zhang ◽  
Shao-Ping Deng
Keyword(s):  
Taste Receptor ◽  
Sweet Taste ◽  
Receptor Model ◽  
Sweet Taste Receptor

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.

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