Research Article: Modulation of Sweet Taste by Umami Compounds via Sweet Taste Receptor Subunit hT1R2

Date Published: April 8, 2015

Publisher: Public Library of Science

Author(s): Jaewon Shim, Hee Jin Son, Yiseul Kim, Ki Hwa Kim, Jung Tae Kim, Hana Moon, Min Jung Kim, Takumi Misaka, Mee-Ra Rhyu, Keiko Abe.

http://doi.org/10.1371/journal.pone.0124030

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.

Partial Text

Most food products comprise of multiple mixtures of tastants. Animals integrate and unify the information regarding each separate taste and decide on their feeding behavior. Much research has focused on and described the interactions between taste modalities [1–4]. However, these studies are restricted to observations of phenotype and phenomenon and the detailed molecular and cellular mechanisms have not been fully investigated.

Although much research has focused on taste-taste interactions, few studies have investigated the combination of sweet and umami tastants. Sako et al. [27] measured the response of the chorda tympani (CT) nerve of rodents to sucrose and MSG either alone or in combination with MSG, and reported that the combination of the sweeteners and MSG exerted synergistic effects. The enhancement was suggested to be due to colocalization of sweet and umami receptors in the same taste receptor cells (TRCs). Kemp and Beauchamp [8] reported changes in other tastes with the application of MSG based on behavioral testing. They showed that at moderate/high concentrations of MSG, sweet and bitter were suppressed; moreover, at a high concentration of MSG, the saltiness of NaCl was enhanced. However, these studies were based on the observation of behaviors and do not provide information regarding the underlying molecular mechanisms.

 

Source:

http://doi.org/10.1371/journal.pone.0124030