抄録
It is reported that T1r2/T1r3 heterodimer plays a role as a sweet taste receptor. Mice lacking T1r3 showed no preference for artificial sweeteners and had diminished but not abolished behavioral and nerve responses to sugars, suggesting that T1r3-independent sweetener binding site also exist in taste cells in mice. However, the numbers and functions of ligand binding sites on T1r2/T1r3 (and/or other sweet receptor) remain largely unknown. In this study, in order to predict the number of sweetener binding site in human, we measured sensitivity thresholds to various sweet taste substances [sucrose, glucose, fructose, saccharin, aspartame, acesulfame-K, glycine, D-phenylalanine, D-tryptophan and L-proline] in human subjects and examined the qualitative similarities among these sweeteners by using a hierarchical cluster analysis. We also used Gymnemic acid and γ-cyclodextrin, which selectively inhibits sweet responses and reduces the inhibitory action of it in human. The ten sweet compounds were classified into five groups [(1) sucrose, glcose and fructose, (2) saccharin, aspartame, acesulfame-K and glycine, (3) D- phenylalanine, (4) D- tryptophan, (5) L- proline]. Four and two single nucleotide polymorphisms with amino acid substitution were detected in T1r2 and T1r3, respectively. These results suggest that there may be at least five different binding sites in human sweet receptor system. The individual differences in sweet sensitivities may be due to these single nucleotide polymorphisms. [J Physiol Sci. 2006;56 Suppl:S183]
