scholarly journals High-resolution genetic mapping of the saccharin preference locus (Sac) and the putative sweet taste receptor (T1R1) gene (Gpr70) to mouse distal Chromosome 4

2001 ◽  
Vol 12 (1) ◽  
pp. 13-16 ◽  
Author(s):  
Xia Li ◽  
Masashi Inoue ◽  
Danielle R. Reed ◽  
Taufiqul Huque ◽  
Ralph B. Puchalski ◽  
...  
Keyword(s):  
High Resolution ◽  
Genetic Mapping ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Chromosome 4 ◽  
Saccharin Preference ◽  
Sweet Taste Receptor ◽  
Distal Chromosome

scholarly journals Genetics of sweet taste preferences

2002 ◽  
Vol 74 (7) ◽  
pp. 1135-1140 ◽  
Author(s):  
Alexander A. Bachmanov ◽  
Danielle R. Reed ◽  
Xia Li ◽  
Gary K. Beauchamp
Keyword(s):  
Positional Cloning ◽  
Inbred Mouse ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Mouse Strains ◽  
Taste Receptors ◽  
Chromosome 4 ◽  
Sweet Taste Receptor ◽  
Distal Chromosome ◽  
Allelic Differences

Inbred mouse strains display marked differences in avidity for sweet solutions due in part to genetic differences among strains. Using several techniques, we have located a number of regions throughout the genome that influence sweetener acceptance. One prominent locus regulating differences in sweetener preferences among mouse strains is the saccharin preference (Sac) locus on distal chromosome 4. Afferent responses of gustatory nerves to sweeteners also vary as a function of allelic differences in the Sac locus, suggesting that this gene may encode a sweet taste receptor. Using a positional cloning approach, we identified a gene (Tas1r3) encoding the third member of the T1R family of putative taste receptors, T1R3. Introgression by serial back-crossing of a chromosomal fragment containing the Tas1r3 allele from the high sweetener-preferring strain onto the genetic background of the low sweetener-preferring strain rescued its low sweetener-preference phenotype. Tas1r3 has two common haplotypes, one found in mouse strains with elevated sweetener preference and the other in strains relatively indifferent to sweeteners. This study, in conjunction with complimentary recent studies from other laboratories, provides compelling evidence that Tas1r3 is equivalent to the Sac locus and that the T1R3 receptor (when co-expressed with taste receptor T1R2) responds to sweeteners. However, other sweetness receptors may remain to be identified.

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.

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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