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Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2.

Shim J, Son HJ, Kim Y, Kim KH, Kim JT, Moon H, Kim MJ, Misaka T, Rhyu MR - PLoS ONE (2015)

Bottom Line: The sensitivity of sucrose to hT1R2/hT1R3 was significantly attenuated by MSG and umami active peptides but not by umami active nucleotides.Application of umami compounds with lactisole, inhibitory drugs that target T1R3, exerted a more severe inhibitory effect.These results suggest that umami peptides affect sweet taste receptors and this interaction prevents sweet receptor agonists from binding to the T1R2 ECD in an allosteric manner, not to the T1R3.

View Article: PubMed Central - PubMed

Affiliation: Division of Creative Food Science for Health, Korea Food Research Institute, Bundang-gu, Sungnam-si, Gyeonggi-do, Republic of Korea.

ABSTRACT
Although the five basic taste qualities-sweet, sour, bitter, salty and umami-can be recognized by the respective gustatory system, interactions between these taste qualities are often experienced when food is consumed. Specifically, the umami taste has been investigated in terms of whether it enhances or reduces the other taste modalities. These studies, however, are based on individual perception and not on a molecular level. In this study we investigated umami-sweet taste interactions using umami compounds including monosodium glutamate (MSG), 5'-mononucleotides and glutamyl-dipeptides, glutamate-glutamate (Glu-Glu) and glutamate-aspartic acid (Glu-Asp), in human sweet taste receptor hT1R2/hT1R3-expressing cells. The sensitivity of sucrose to hT1R2/hT1R3 was significantly attenuated by MSG and umami active peptides but not by umami active nucleotides. Inhibition of sweet receptor activation by MSG and glutamyl peptides is obvious when sweet receptors are activated by sweeteners that target the extracellular domain (ECD) of T1R2, such as sucrose and acesulfame K, but not by cyclamate, which interact with the T1R3 transmembrane domain (TMD). Application of umami compounds with lactisole, inhibitory drugs that target T1R3, exerted a more severe inhibitory effect. The inhibition was also observed with F778A sweet receptor mutant, which have the defect in function of T1R3 TMD. These results suggest that umami peptides affect sweet taste receptors and this interaction prevents sweet receptor agonists from binding to the T1R2 ECD in an allosteric manner, not to the T1R3. This is the first report to define the interaction between umami and sweet taste receptors.

No MeSH data available.


The inhibitory effect by umami compounds was dependent on the sweet receptor agonist.The responses of hT1R2/hT1R3-expressing cells were measured after co-application of umami compounds (30 mM MSG and 1 mM Glu-Glu) with other agonist; acesulfame K (A), aspartame (B) or cyclamate (C). Inhibitory effect of sweet receptor by MSG or umami dipeptide (Glu-Glu) was not shown at induction by aspartame or cyclamate. Asterisk *, **, *** stands for p<0.05, p<0.01, p<0.001, respectively.
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pone.0124030.g002: The inhibitory effect by umami compounds was dependent on the sweet receptor agonist.The responses of hT1R2/hT1R3-expressing cells were measured after co-application of umami compounds (30 mM MSG and 1 mM Glu-Glu) with other agonist; acesulfame K (A), aspartame (B) or cyclamate (C). Inhibitory effect of sweet receptor by MSG or umami dipeptide (Glu-Glu) was not shown at induction by aspartame or cyclamate. Asterisk *, **, *** stands for p<0.05, p<0.01, p<0.001, respectively.

Mentions: To investigate whether MSG and umami-dipeptide inhibit agonist—receptor binding, we tested three other sweet receptor agonists: acesulfame K, aspartame and cyclamate. Acesulfame K and aspartame activate the sweet receptor in the ATD of T1R2, whereas cyclamate affects the TMD of T1R3. Induction of sweet receptor cells by acesulfame K was inhibited by Glu-Glu and MSG, similar to sucrose (Fig 2A). Compared with these agonists, treatment of Glu-Glu, MSG did not inhibit the cyclamate- or aspartame-induced response of sweet receptor cells (Fig 2B and 2C). Although aspartame affects the ATD of T1R2, a recent study suggested that aspartame uses different binding sites than acesulfame K [19]. These results suggest that MSG and umami dipeptides affect specific regions of the ATD of T1R2 to inhibit agonist binding.


Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2.

Shim J, Son HJ, Kim Y, Kim KH, Kim JT, Moon H, Kim MJ, Misaka T, Rhyu MR - PLoS ONE (2015)

The inhibitory effect by umami compounds was dependent on the sweet receptor agonist.The responses of hT1R2/hT1R3-expressing cells were measured after co-application of umami compounds (30 mM MSG and 1 mM Glu-Glu) with other agonist; acesulfame K (A), aspartame (B) or cyclamate (C). Inhibitory effect of sweet receptor by MSG or umami dipeptide (Glu-Glu) was not shown at induction by aspartame or cyclamate. Asterisk *, **, *** stands for p<0.05, p<0.01, p<0.001, respectively.
© Copyright Policy
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC4390298&req=5

pone.0124030.g002: The inhibitory effect by umami compounds was dependent on the sweet receptor agonist.The responses of hT1R2/hT1R3-expressing cells were measured after co-application of umami compounds (30 mM MSG and 1 mM Glu-Glu) with other agonist; acesulfame K (A), aspartame (B) or cyclamate (C). Inhibitory effect of sweet receptor by MSG or umami dipeptide (Glu-Glu) was not shown at induction by aspartame or cyclamate. Asterisk *, **, *** stands for p<0.05, p<0.01, p<0.001, respectively.
Mentions: To investigate whether MSG and umami-dipeptide inhibit agonist—receptor binding, we tested three other sweet receptor agonists: acesulfame K, aspartame and cyclamate. Acesulfame K and aspartame activate the sweet receptor in the ATD of T1R2, whereas cyclamate affects the TMD of T1R3. Induction of sweet receptor cells by acesulfame K was inhibited by Glu-Glu and MSG, similar to sucrose (Fig 2A). Compared with these agonists, treatment of Glu-Glu, MSG did not inhibit the cyclamate- or aspartame-induced response of sweet receptor cells (Fig 2B and 2C). Although aspartame affects the ATD of T1R2, a recent study suggested that aspartame uses different binding sites than acesulfame K [19]. These results suggest that MSG and umami dipeptides affect specific regions of the ATD of T1R2 to inhibit agonist binding.

Bottom Line: The sensitivity of sucrose to hT1R2/hT1R3 was significantly attenuated by MSG and umami active peptides but not by umami active nucleotides.Application of umami compounds with lactisole, inhibitory drugs that target T1R3, exerted a more severe inhibitory effect.These results suggest that umami peptides affect sweet taste receptors and this interaction prevents sweet receptor agonists from binding to the T1R2 ECD in an allosteric manner, not to the T1R3.

View Article: PubMed Central - PubMed

Affiliation: Division of Creative Food Science for Health, Korea Food Research Institute, Bundang-gu, Sungnam-si, Gyeonggi-do, Republic of Korea.

ABSTRACT
Although the five basic taste qualities-sweet, sour, bitter, salty and umami-can be recognized by the respective gustatory system, interactions between these taste qualities are often experienced when food is consumed. Specifically, the umami taste has been investigated in terms of whether it enhances or reduces the other taste modalities. These studies, however, are based on individual perception and not on a molecular level. In this study we investigated umami-sweet taste interactions using umami compounds including monosodium glutamate (MSG), 5'-mononucleotides and glutamyl-dipeptides, glutamate-glutamate (Glu-Glu) and glutamate-aspartic acid (Glu-Asp), in human sweet taste receptor hT1R2/hT1R3-expressing cells. The sensitivity of sucrose to hT1R2/hT1R3 was significantly attenuated by MSG and umami active peptides but not by umami active nucleotides. Inhibition of sweet receptor activation by MSG and glutamyl peptides is obvious when sweet receptors are activated by sweeteners that target the extracellular domain (ECD) of T1R2, such as sucrose and acesulfame K, but not by cyclamate, which interact with the T1R3 transmembrane domain (TMD). Application of umami compounds with lactisole, inhibitory drugs that target T1R3, exerted a more severe inhibitory effect. The inhibition was also observed with F778A sweet receptor mutant, which have the defect in function of T1R3 TMD. These results suggest that umami peptides affect sweet taste receptors and this interaction prevents sweet receptor agonists from binding to the T1R2 ECD in an allosteric manner, not to the T1R3. This is the first report to define the interaction between umami and sweet taste receptors.

No MeSH data available.