Molecular Genetic Identification of a Candidate Receptor Gene for Sweet Taste

Kitagawa, Masae; Kusakabe, Yuko; Miura, Hirohito; Ninomiya, Yuzo; Hino, Akihiro

doi:10.1006/bbrc.2001.4760

Cited by 299 publications

(186 citation statements)

References 25 publications

(24 reference statements)

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“…Sweet tastants, including artificial sweeteners, bind to a heterodimer of the G protein-coupled receptors, T1R2 and T1R3. [28][29][30][31][32][33] Similarly, umami tastants bind to a dimer of T1R1 and T1R3. 34,35 Stimuli that give rise to bitter taste perception are known to bind with members from the T2R family of receptor proteins.…”

Section: Taste Bud Anatomy and Physiologymentioning

confidence: 99%

Taste perception, associated hormonal modulation, and nutrient intake

et al. 2015

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It is well known that taste perception influences food intake. After ingestion, gustatory receptors relay sensory signals to the brain, which segregates, evaluates, and distinguishes the stimuli, leading to the experience known as "flavor." It is well accepted that five taste qualities -sweet, salty, bitter, sour, and umami -can be perceived by animals. In this review, the anatomy and physiology of human taste buds, the hormonal modulation of taste function, the importance of genetic chemosensory variation, and the influence of gustatory functioning on macronutrient selection and eating behavior are discussed. Individual genotypic variation results in specific phenotypes of food preference and nutrient intake. Understanding the role of taste in food selection and ingestive behavior is important for expanding our understanding of the factors involved in body weight maintenance and the risk of chronic diseases including obesity, atherosclerosis, cancer, diabetes, liver disease, and hypertension.

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Section: Taste Bud Anatomy and Physiologymentioning

confidence: 99%

Taste perception, associated hormonal modulation, and nutrient intake

et al. 2015

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“…The Sac locus has been mapped to the subtelomeric region of mouse chromosome 4 (Phillips et al, 1994;Lush et al, 1995;Bachmanov et al, 1997;Blizard et al, 1999;Li et al, 2001) and more recently has been cloned positionally . It corresponds to the Tas1r3 gene, which encodes a sweet taste receptor, T1R3 (Kitagawa et al, 2001;Max et al, 2001;Montmayeur et al, 2001;Nelson et al, 2001;Sainz et al, 2001;Li et al, 2002a;Nelson et al, 2002;Ariyasu et al, 2003;Damak et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in the Taste Receptor Gene (Tas1r3) Region Are Associated with Saccharin Preference in 30 Mouse Strains

Reed

Li²,

Li³

et al. 2004

J. Neurosci.

163

146

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The results of recent studies suggest that the mouse Sac (saccharin preference) locus is identical to the Tas1r3 (taste receptor) gene. The goal of this study was to identify Tas1r3 sequence variants associated with saccharin preference in a large number of inbred mouse strains. Initially, we sequenced ϳ6.7 kb of the Tas1r3 gene and its flanking regions from six inbred mouse strains with high and low saccharin preference, including the strains in which the Sac alleles were described originally (C57BL/6J, Sac b ; DBA/2J, Sac d ). Of the 89 sequence variants detected among these six strains, eight polymorphic sites were significantly associated with preferences for 1.6 mM saccharin. Next, each of these eight variant sites were genotyped in 24 additional mouse strains. Analysis of the genotype-phenotype associations in all 30 strains showed the strongest association with saccharin preference at three sites: nucleotide (nt) Ϫ791 (3 bp insertion/deletion), nt ϩ135 (Ser45Ser), and nt ϩ179 (Ile60Thr). We measured Tas1r3 gene expression, transcript size, and T1R3 immunoreactivity in the taste tissue of two inbred mouse strains with different Tas1r3 haplotypes and saccharin preferences. The results of these experiments suggest that the polymorphisms associated with saccharin preference do not act by blocking gene expression, changing alternative splicing, or interfering with protein translation in taste tissue. The amino acid substitution (Ile60Thr) may influence the ability of the protein to form dimers or bind sweeteners. Here, we present data for future studies directed to experimentally confirm the function of these polymorphisms and highlight some of the difficulties of identifying specific DNA sequence variants that underlie quantitative trait loci.

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“…For example, KO mice lacking T1r3 still respond to multiple sugars, particularly glucose (11). In addition to Sac/Tas1r3, there are multiple quantitative trait loci that contribute importantly to sweet taste responses in mice (3,18). Physiological studies with canine lingual epithelium identified sugar-activated cation currents proposed to function as a sweet receptor (19)(20)(21).…”

mentioning

confidence: 99%

Glucose transporters and ATP-gated K ⁺ (K _ATP ) metabolic sensors are present in type 1 taste receptor 3 (T1r3)-expressing taste cells

Yee

Sukumaran

Kotha

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

183

178

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Although the heteromeric combination of type 1 taste receptors 2 and 3 (T1r2 + T1r3) is well established as the major receptor for sugars and noncaloric sweeteners, there is also evidence of T1r-independent sweet taste in mice, particularly so for sugars. Before the molecular cloning of the T1rs, it had been proposed that sweet taste detection depended on ( a ) activation of sugar-gated cation channels and/or ( b ) sugar binding to G protein-coupled receptors to initiate second-messenger cascades. By either mechanism, sugars would elicit depolarization of sweet-responsive taste cells, which would transmit their signal to gustatory afferents. We examined the nature of T1r-independent sweet taste; our starting point was to determine if taste cells express glucose transporters (GLUTs) and metabolic sensors that serve as sugar sensors in other tissues. Using RT-PCR, quantitative PCR, in situ hybridization, and immunohistochemistry, we determined that several GLUTs (GLUT2, GLUT4, GLUT8, and GLUT9), a sodium–glucose cotransporter (SGLT1), and two components of the ATP-gated K + (K ATP ) metabolic sensor [sulfonylurea receptor (SUR) 1 and potassium inwardly rectifying channel (Kir) 6.1] were expressed selectively in taste cells. Consistent with a role in sweet taste, GLUT4, SGLT1, and SUR1 were expressed preferentially in T1r3-positive taste cells. Electrophysiological recording determined that nearly 20% of the total outward current of mouse fungiform taste cells was composed of K ATP channels. Because the overwhelming majority of T1r3-expressing taste cells also express SUR1, and vice versa, it is likely that K ATP channels constitute a major portion of K + channels in the T1r3 subset of taste cells. Taste cell-expressed glucose sensors and K ATP may serve as mediators of the T1r-independent sweet taste of sugars.

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Molecular Genetic Identification of a Candidate Receptor Gene for Sweet Taste

Cited by 299 publications

References 25 publications

Taste perception, associated hormonal modulation, and nutrient intake

Taste perception, associated hormonal modulation, and nutrient intake

Polymorphisms in the Taste Receptor Gene (Tas1r3) Region Are Associated with Saccharin Preference in 30 Mouse Strains

Glucose transporters and ATP-gated K ⁺ (K _ATP ) metabolic sensors are present in type 1 taste receptor 3 (T1r3)-expressing taste cells

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Molecular Genetic Identification of a Candidate Receptor Gene for Sweet Taste

Cited by 299 publications

References 25 publications

Taste perception, associated hormonal modulation, and nutrient intake

Taste perception, associated hormonal modulation, and nutrient intake

Polymorphisms in the Taste Receptor Gene (Tas1r3) Region Are Associated with Saccharin Preference in 30 Mouse Strains

Glucose transporters and ATP-gated K + (K ATP ) metabolic sensors are present in type 1 taste receptor 3 (T1r3)-expressing taste cells

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Glucose transporters and ATP-gated K ⁺ (K _ATP ) metabolic sensors are present in type 1 taste receptor 3 (T1r3)-expressing taste cells